The New York Academy of Sciences, the Warren Alpert Medical School of Brown University, and the University of Massachusetts, Boston are planning a landmark international program, "Behavioral Epigenetics", to explore how environmental factors can affect alterations in behavior by biochemically changing the function of genes or gene expression without affecting the basic gene structure. The principal investigator for this grant is Dr. Barry Lester, Professor of Psychiatry and Human Behavior and Professor of Pediatrics at the Warren Alpert Medical School of Brown University, and Director of the Brown Center for the Study of Children at Risk. The program, one of the first major meetings focused on Behavioral Epigenetics, will include a 2-day CME-accredited conference (October 29-30, 2010, Boston) and high-quality enduring materials to disseminate the scientific information exchanged by participants. For background participants will review the history and describe the field of epigenetics, role in normal embryological and fetal development, basic mechanisms and processes including biochemical, cellular, gene transcription and expression, and relations to fetal programming and neural plasticity and they also will discuss medical outcomes and research on behavioral effects of epigenetic processes. However the primary focus will be on epigenetic functioning and behavioral outcomes including learning, memory, mental illness, normal development and developmental psychopathology. Prenatal and postnatal factors that produce epigenetic changes in behavior, and the intergenerational transfer and reversibility of these effects will be also considered. Participants will also brainstorm about pending questions and future steps. It is anticipated that the multidisciplinary discussions originating from this symposium, their dissemination through enduring materials, and the collaborations emerging from this forum will foster advancements in the field of Behavioral Epigenetics, and will improve the understanding of 1) the fundamental mechanisms that shape behavior, its development and epigenetic modulation, 2) individual vulnerability and resilience to adverse behavioral outcome;and 3) development of targeted therapies for malfunctions in epigenetic modulation. To achieve these goals, the conference agenda will incorporate two plenary sessions per day (three speakers per session) and ample time for panel and audience discussion to encourage networking and audience participation. Networking breaks will be available, including an evening reception concurrent with a poster session that will allow young scientists to showcase their work. The conference will attract wide participation (250-300 attendees) among senior investigators, physicians, post-doctoral and clinical fellows, students and industry scientists working on neuroscience, normal and/or pathological embryonic, fetal, childhood, adolescent and reproductive development, behavioral sciences, mental health, drug addition, cell and molecular biology, genetics, genomics, proteomics, and drug discovery, among others. PUBLIC HEALTH RELEVANCE: The two-day CME-accredited scientific conference will provide a neutral forum to discuss recent advancements, challenges, and future steps in research exploring how environmental factors affect behavioral outcomes (learning, memory, mental illness, normal development and developmental psychopathology) via epigenetic modulation. The cross-disciplinary discussions among participants, their dissemination through enduring materials, and the new research and collaborations generated at the meeting will help delineate the field of Behavioral Epigenetics, and foster advancement in our understanding of mechanisms shaping epigenetic changes on gene function and expression, and individual vulnerability and resilience to adverse behavioral outcome. It is anticipated that this symposium will explore possibilities for new therapeutic applications of epigenetics to treat patients with depression, addiction, schizophrenia, and other neuro-developmental disorders which may in part result from malfunctions in epigenetic modulation.